Read e-book online Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy PDF

By Santiago Grisolía, Vicente Felipo

ISBN-10: 1461360587

ISBN-13: 9781461360582

ISBN-10: 1461524849

ISBN-13: 9781461524847

This quantity includes the papers provided within the foreign summer season path on "Cirrhosis, Hyperammonemia and Hepatic Encephalopathy," which used to be one of many prestigious summer season path, of the Complutense collage of Madrid held in EI Escorial, Spain, in the course of August 10-14, 1992. Liver cirrhosis is likely one of the major explanations of demise in western nations. moreover there's a sequence of liver dysfunctions together with fulminant hepatic failure, Reye's syndrome and congenital defects of urea cycle enzymes that can result in hepatic encephalopathy, coma and demise. because of impaired liver functionality, the facility to detoxify ammonia by way of its incorporation into urea is diminshed, leading to elevated ammonia degrees in blood and mind. Hyperammonemia is taken into account one of many major elements within the mediation of hepatic encephalopathy and the classical medical remedies are directed in the direction of lowering blood ammonia degrees. part of the e-book is for that reason dedicated to the learn of sure features of ammonia metabolism corresponding to the legislation of the urea cycle, the most mechanism of ammonia cleansing in mammals, that is situated almost always within the liver. The metabolism of ammonia in different tissues, together with mind, can also be provided, in addition to the results of hyperammonemia on mind metabolism and serve as and on mind microtubules. The keep watch over of cerebral protein breakdown is reviewed. The classical and a few lately proposed medical remedies in addition to dietary issues within the administration of sufferers with liver failure also are discussed.

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Extra resources for Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy

Example text

For simplicity only the nitrogen is traced. An excellent quantitative analysis of amino acid oxidation and related gluconeogenesis has recently been published (58). The fate of the amino carbon is discussed in great detail in this review, so only a few points concerning the fate of amino acid carbon will be made here. Most of the amino acids that arise from digestion of dietary protein and that are not required for protein synthesis and other biosynthetic processes are oxidized in the liver. Oxidation of amino acids provides the liver with 50% of its energy needs (58).

J. Physiol. 393:283 - 305 . 74. , 1989 Physiologic importance of glutamine. Metabolism: 38 Suppl. 1: - 5. 75. , 1992 Glutamine metabolism by heart muscle. Properties of phosphate-activated glutaminase. Biochem. J. 282:559 - 564. 76. H. M. , 1976 Alterations of myocardial amino acid metabolism in chronic ischemic heart disease. J. Clin. Invest. 58:1185 - 1192. 77. , 1983 Cerebral ammonia metabolism in vivo. In: Glutamine, Glutamate and GABA in the Central Nervous System, edited by L. Hertz, E. G.

Glutamine accounts for about 20% and 67%, respectively, of the amino acid content of human plasma and CSF (21). The widespread occurence of glutamine synthetase probably accounts for the high concentration of glutamine in most body tissues. Glutamine acts as a non-toxic carrier of ammonia, and the amide nitrogen (and to a lesser extent the amine nitrogen) is used in a large number of biosynthetic reactions. These reactions are summarized in Figure 1. Additionally, glutamine is a major energy source of small intestine (22), bone (23), and human diploid fibroblasts (24), and may contribute to energy metabolism in the kidney (25).

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Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy by Santiago Grisolía, Vicente Felipo


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